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CP2 Child Health > Nephrology > Flashcards

Nephrology Flashcards

1
Q

ACUTE NEPHRITIS: Outline the aetiology, clinical features and management.

A

Aetiology: Accumulation of immune complexes at the GBM causes inflammation of the membrane and endothelial proliferation. In short, this leads to reduced glomerular perfusion/filtration.

There are autoimmune, infectious and hereditary causes.

Common causes: Post-streptococcal infection, vasculitis (HSP, granulomatosis with polyangiitis, SLE, microscopic polyangitis), IgA nephropathy a.k.a. Berger’s, Goodpasture’s disease

Clinical features:

  • Hypertension (→ seizures)
  • Oedema (periorbital)
  • Haematuria and proteinuria
  • Renal dysfunction. leading to:
    • Oliguria
    • Volume overload ( = oedema)

Management:

Supportive care as resolution is often spontaneous

  • Fluid restriction with use of diuretics when necessary, prophylactic antibiotics
  • Monitoring urine output

Monitoring of renal function to check for damage

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2
Q

ACUTE NEPHRITIS: Be aware of the long term complications of HSP

A
  • Renal impairment
    • Follow-up appointment after HSP diagnosis to check blood pressure, urine dip ( check for proteinuria) and for any signs of renal impairment.
    • Follow-up with the GP at regular intervals to complete the above (timing dependent upon +/- proteinuria at time of presentation)
  • Severe proteinuria may lead to nephrotic syndrome
  • Progressive chronic kidney disease: Hypertension, heavy proteinuria, oedema and declining renal function are all seen
  • Intussception
    • ! WARN about red currant jelly stools
  • Ileus
  • Orchitis
  • Testicular torsion/haemorrhage

Intussception, ileus and orchitis are rare complications

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3
Q

ACUTE NEPHRITIS: Outline the management plan of patients with HSP including follow-up for detection of HSP nephritis.

*Consider the triad of symptoms*

A

TRIAD OF SYMPTOMS: Arthalgia (knees, ankles), purpuric rash, colicky abdominal pain (+/- diarrhoea, haematemesis, obstruction)

Classically affects children between the ages of 3 - 10 years

Child is usually clinically well - unlike meningococcal disease

Preceeded by an illness or vaccination

Management

Arthalgia: NSAIDs

CAUTION If there is renal involvement then be wary of NSAID use

Rehydration with fluid balance monitoring

?Low dose corticosteroids - no evidence of benefit in terms of reducing risk of renal complications

Year long follow-up to check blood pressure and urinalysis

  • Renal involvement is often delayed, with renal detriment seen after resolution of the rash (4/52)
  • Hypertension and proteinuria indicate renal pathology and need for specilaist referral
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4
Q

ACUTE NEPHRITIS: Name the most common cause of acute glomerulonephritis in childhood.

A
  • Post-infectious
    • Group A Streptococcus
  • Vasculitis
    • HSP (IgA vasculitis - IgA and IgG accumulate at the GBM, causing complement activation. Precipitates an inflammatory response with vasculitis)
    • SLE
    • Granulomatosis with polyangiitis
  • IgA nephropathy (Berger’s)
  • Mesangiocapillary glomerulonephritis
  • Goodpasture syndrome
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5
Q

ACUTE NEPHRITIS: List the initial investigations in patients presenting with acute Glomerulonephritis

A
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6
Q

ACUTE NEPHRITIS: Be aware that IgA nephropathy shares the histopathological features of HSP nephritis

A

Histopathological features:

  • IgA deposition
  • Endothelial proliferation at the glomerulus

Differentiating factors

  • Systemic involvement in HSP (joints, GI, skin), only renal in IgA nephropathy
  • HSP is more commonly seen in younger children (3-10 years), IgA nephropathy is more common between the ages of 15 - 30
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7
Q

NEPHROTIC SYNDROME: Know the aetiology, incidence and presenting features of childhood nephrotic syndrome.

A

Aetiology: Dysfunction of the GBM leads to heavy proteinuria

  • Secondary to systemic disease
    • HSP, SLE, malaria, bee sting
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
  • Membranoproliferative glomerulonephritis

Incidence:

Usually seen between 2-6 years

Presenting features:

  • Oedema
  • Proteinuria (> 1g/m2/day or 3+ of protein on dipstick)
  • Hypoalbuminaemia
  • Hyperlipidaemia

Clinical features

  • Oedema: Most often periorbital up on waking, swollen lips
  • Oedema of the scrotum/vulva, ankles and legs
  • Infections (due to loss of immunoglobulins in the urine)
  • Ascites
  • Foamy urine
  • Discomfort relating to swelling or skin breakdown
  • Weight gain
  • Abdominal distension
  • Tiredness
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8
Q

NEPHROTIC SYNDROME: Name the most common type in childhood

A
  • 80% of cases are due to minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous nephropathy
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9
Q

NEPHROTIC SYNDROME: Outline the initial management of children who present with nephrotic syndrome.

A

High dose corticosteroids for 4/52, with dose weaning

  • MONITOR blood pressure - hypertension is a recognised complication

Dietary sodium restriction: Helps to reduce fluid retention

Prophylactic antibiotics: To reduce infection risk (2º to loss of immunoglobulins)

Fluid management: Diuretic therapy and IV albumin may be required

Vaccination: Pneumococcal vaccination and varicella immunisation should be considered

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10
Q

NEPHROTIC SYNDROME: Be aware of the atypical features which would prompt consideration of second line treatment and/or a renal biopsy.

A

Nephrotic syndrome unresponsive to steroid treatment or frequent relapse indicates the need for a renal biopsy, prior to commencing immunomodulatory agents.

Atypical features that suggest that the aetiology is unlikely to be minimal change disease (hence likely to be steroid unresponsive)

  • Age < 1 or > 12 years
  • Gradual onset of oedema
  • Macroscopic haematuria
  • Rash/features of systemic disease
  • Hypocomplementaemia
  • Renal dysfunction
  • Steroid resistance with failure to respond to steroids by 4 weeks
  • Significant hypertension
  • Confirmation of calcineurin nephrotoxicity
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11
Q

UTI: Know the incidence and common organisms which cause childhood UTI.

A

Incidence

  • 1/10 girls, 1/30 boys have a UTI before the age of 16

Causative microorganisms

  • E.Coli
  • Proteus
  • Klebsiella
  • Enterococcus
  • Pseudomonas: May indicate a structural abnormality
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12
Q

UTI: Reach a differential diagnosis for children presenting with haematuria.

A

UTI

Nephritis – nephritic syndrome

Urinary system trauma

Renal calculi

Congenital abnormality e.g. stricture

Renal malignancy

Bleeding disorders

Hypercalciuria

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13
Q

UTI: List the presenting features of UTI in infants, preverbal children and verbal children.

A
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14
Q

UTI: Know methods of collecting urine i.e. clean catch urine, bag urine, catheter specimen and suprapubic aspirate and be aware of some of the advantages and disadvantages of each meth

A
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15
Q

UTI: List the criteria for diagnosis of UTI based on urine dipstick and urine culture

A

Diagnosis from urine culture

  • > 105 organisms/mL in pure growth and clinical suspicion
  • Any growth from suprapubic aspirate

Diagnosis from urine dipstick

(see image)

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16
Q

UTI: Know the definition of atypical UTI and recurrent UTI as stated in the NICE guideline CG54 (Childhood UTI) and outline the investigation schedule based on these definitions.

A

Atypical UTI:

  • Seriously ill
  • Poor urine output (? congenital abnormality)
  • Abdomial/renal mass
  • Raised creatinine
  • Sepitcaemia
  • Failure to respond to antibiotic therapy within 48 hours
  • Causative agent not E.Coli

Recurrent UTI:

  • 2 or more upper UTIs OR
  • 1 upper and 1 lower UTI OR
  • 3 lower UTIs

Investigations:

  • Age dependent
    • ​Renal USS is indicated for children < 6 months presenting with first UTI, children > 6 months with features of an atypical UTI and children with recurrent UTIs
  • Atypical UTI:
    • USS during acute infection for all age groups
    • DMSA and KUB scan after infection for those < 6 months old
  • Recurrent UTI
    • USS during acute infection for those < 6 months
    • DMSA (4/6 months) after the infection
      • Assess for the presence of renal scarring
    • MCUG for those < 6 months
      • May allow for posterior urethral valves (in males) or VUR to be detected
17
Q

UTI: Know the incidence of Vesicoureteric Reflux (VUR) in the general population and in children who present with a UTI.

A

Incidence

General population - 1%

Children presenting with UTI - 30-45% of < 5s

18
Q

UTI: Outline the diagnostic tests for VUR

A

Antenatal scans: Small, smooth kidneys

MCUG: Catheterisation to allow introduction of a contrast dye into the bladder. The flow of dye in the urine is checked using radiography (X-ray). Dye will travel contralaterally in reflux

Indirect cystogram: Injection of radioactive isotope, which is then taken up by the kidneys. The flow is then analysed by asking the child to urinate in front of a detector. Only suitable for children who are able to mictuate on demand

19
Q

UTI: Define pyelonephritis and cystitis as stated in the NICE guideline CG54 (Childhood UTI)

*think of definitive signs/symptoms*

A

Pyelonephritis:

  • Bacteriuria
  • Fever (> 38ºC)

OR

  • Fever < 38ºC with loin pain/tenderness

?Elevated CRP

Cystitis:

  • Bacteriuria WITHOUT systemic signs/symptoms
20
Q

UTI: Be aware of the treatment of Pyelonephritis.

A
  • Immediate referral to paediatrics for infants less than 3 months of age
  • Analgesia
  • Ensure adequate hydration
  • Antibiotic therapy
    • PO: Cefalexin, coamoxiclav
    • IV: Coamoxiclav
21
Q

UTI: Understand that Vulvo-vaginitis is common in young girls and the initial steps in management.

A

Vulvo-vaginitis: Inflammation of the vagina and vulva

Signs/symptoms: Erythema, pruritis, pain, discharge (yellow/green)

Pathophysiology: The lower levels of sex hormones in younger females mean the genital skin is thinner and less acidic, creating a predisposition to infection.

Initial steps in management:

  • Further investigations, namely swabs, may be indicated if the conditon is causing distress
  • Personal hygiene adjustments: Wipe front to back, wash the genitals after urination/opening the bowels
  • Clothing: Avoid tight fitting trousers and wearing underwear at night
  • Acitivities: Avoid direct pressure on the vulva, avoid chlorinated water
  • Relief from soreness: Apply a cold compress, application of sudocrem/bepanthen
22
Q

AKI: Know the presenting features of acute kidney injury (AKI) in childhood.

A
  • Reduced urine output (< 0.5 ml/kg/hr for 8 hours)
  • Increased serum creatinine
    • ​Increase from baseline or value greater x1.5 the upper limit for the age group
  • Systemically unwell child (PEWS)

​

23
Q

AKI: Name the most common causative organism of childhood diarrhoea associated Haemolytic Uraemic Syndrome (HUS)

A

Verocytotoxin-producting E.coli O157:H7 (VTEC)

  • Acquired through contact with farm animals or eating uncooked beef

Less commonly, HUS may be seen as a consequence of Shigella infection

24
Q

AKI: List the triad of abnormalities which define HUS

A
  1. Acute kidney injury
  2. Haemolytic anaemia
  3. Thrombocytopenia

The E.coli preferentially localises to the kidney and causes intravascular thrombogenesis, leading to AKI. This depletes platelets, leading to thrombocytopenia, and RBC become damaged as they circulate through the occluded vessels, promopting their lysis.

25
Q

AKI: Appreciate the difference between diarrhoea associated and non-diarrhoea associated HUS and the implications for prognosis

A

Diarrhoea associated HUS:

  • Prodrome of blood diarrhoea
  • With early support therapy, including dialysis, prognosis is usually good
  • However, long-term follow-up is necessary as there may be persistent proteinuria and the development of hypertension, with progression to CKD in subsequent years

Non-diarrhoea associated HUS:

  • No diarrhoeal prodrome
  • May be familial and frequently relapses
  • Prognosis is poorer as there is a high risk of hypertension and progressive CKD.
  • New treatment with monoclonal antibodies has improved prognosis
26
Q

CHRONIC KIDNEY DISEASE: List the 5 stages of chronic kidney disease

A
27
Q

CHRONIC KIDNEY DISEASE: Name the most common cause of glomerulonephritis in childhood

A
  • Post-streptococcal glomerulonephritis
    • Streptococcal throat/skin infection
  • Autoimmune conditions: lupus, Goodpasture’s syndrome, granulomatosis with polyangiitis
28
Q

CHRONIC KIDNEY DISEASE: List the initial investigations in patients presenting with acute glomerulonephritis

A
  • Urine dip: Check for the presence of blood and protein within the urine
  • Check BP
  • MC&S: To look for infective causes
  • Investigation of recent streptococcal infection:
    • Raised ASO/anti-DNAse B titre, low complement C3 (and C4) that return to normal after 3-4 weeks
    • Throat swab
  • U&Es, FBC, LFTs and albumin: Allows electrolyte disturbances and hypoalbuminaemia to be detected. Checks for blood loss and anaemia
  • ESR
  • Renal USS: To identify any parenchymal abnormalities
  • Auto-antibody tests: Elevated ANA and dsDNA may suggest SLE
  • Renal biopsy
29
Q

HYPERTENSION: Understand the importance of blood pressure centiles in children

A

Blood pressure increases with age and height in paediatrics and should be plotted on a centile chart.

Hypertension is BP above the 95th percentile for height, age and sex.

30
Q

HYPERTENSION: Be aware of the common causes of hypertension in children

A
  • Renal
    • Renal parenchymal disease
    • Renovascular e.g. renal artery stenosis
    • Polycystic kidney disease
    • Renal tumours
  • Cardiac
    • ​Coarctation of the aorta
  • Catecholamine excess
    • ​Pheochromocytoma
    • Neuroblastoma
  • Endocrine
    • ​Congenital adrenal hyperplasia
    • Cushing syndrome/corticosteroid therapy
    • Hyperthyroidism
  • Essential hypertension
31
Q

HYPERTENSION: Understand the importance of investigation for an underlying cause in children who present with hypertension

A

Minimises the risk of end organ damage.

Allows for correction, if possible.

32
Q

URINARY TRACT ABNORMALITIES: Know the presenting features of urinary tract abnormalities

A

Antenatal diagnosis:

  • Renal agenesis (→ oligohydramnios): Leads to Potter sydrome (characteristic facies, lung hypoplasia and postural deformities)
  • Hydronephrosis, indicative of urinary flow obstruction :
    • Bladder neck, PUJ or VUJ obstruction
    • Posterior urethral valves (PUV)
    • Consider which would lead to uni/bilateral hydronephrosis
  • Multicystic dysplastic kidney
    • May occur due to failed fusion of the ureteric bud, leading to failure of kidney formation and function. May be uni or bilateral. Bilateral multicystic dysplastic kidneys lead to Potter syndrome.
    • Polycystic kidney disease and tuberous sclerosis, in both these conditions some renal function is retained
  • Pelvic kidney or horseshoe kidney
  • Duplex system:
  • Bladder exstrophy: Due to failed fusion of midline structures. Exposed bladder mucosa results.

UTI: Particularly in children < 3/12 and recurrent UTIs

33
Q

URINARY TRACT ABNORMALITIES: Understand the investigations used in the diagnosis of antenatal urinary tract abnormalities

A
  • Ultrasound scan
34
Q

URINARY TRACT ABNORMALITIES: Outline the embryology and be aware of the treatment for hypospasias

A

Embryology of hypospadias:

Resultant of failed fusion of the urethral groove, causing displacement of the external urethral meatus opening.

Treatment:

  • Surgical correction
35
Q

NEUROPATHIC BLADDER: Have an awareness of the presenting features of children with neuropathic bladder

A
  • Incontinence: Overflow
  • Recurrent UTIs: Secondary to urinary stasis
  • Kidney injury
  • Nephrolithiasis

CP2 Child Health (6 decks)

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